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The Endocrine System in Overtraining

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 27 The Endocrine System in Overtraining

Ann C. Snyder, PHD

and Anthony C. Hackney, PHD, DSC
CONTENTS
Introduction
Endocrine Function and the Overtraining Syndrome
Other Hypothesized Mechanisms of the Overtraining
Syndrome
Training Considerations to Prevent the Overtraining
Syndrome
References

INTRODUCTION
An athlete’s main goal is to perform well and presumptively win competitions. As
such, most athletes are never satisfied if they are not performing to their best and obtain-
ing personal records. Because of this performance drive, athletes can train extensively
hard in spite of everything else happening in their lives, to the point of overtraining.
Overtraining has been defined as an imbalance between the training stress, including
other life stresses, and the recovery or regeneration process (1–5). While scientists and
sports medicine professionals know that overtraining occurs in athletes, most of the
knowledge and/or information concerning it comes primarily from personal experience,
case studies, and short-term experimental investigations, none of which because of
methodological limitations have added substantially to the scientific literature as will be
seen during this chapter. When an athlete becomes overtrained, it will usually take
months if not years to recover (6–8); thus it would be highly unethical to deliberately
overtrain an athlete just for science sake; therefore, scientists have very little long-term
training information (8). In spite of this lack of direct scientific information, much work
has been performed to examine, predict, and prevent overtraining in athletes, and this
chapter will examine some of this work especially as it relates to the endocrine system
and the current proposed mechanisms.

From: Endocrinology of Physical Activity and Sport: Second Edition

Edited by: N. Constantini and A.C. Hackney, DOI 10.1007/978-1-62703-314-5_27
© Springer Science+Business Media New York 2013

523
524 Snyder and Hackney

In 1936, Selye (9) described the general adaptation syndrome (GAS) which proposes
how individuals will adapt to stress if it is not too great. According to Selye (9) the GAS
has three phases: an alarm phase (where the body recognizes a stressor and responds to
it), the resistance phase (where physiological adaptations occur which results in an
enhanced level of homeostasis), and the exhaustion phase (where adaptation is not pos-
sible because the body is overwhelmed, and if prolonged enough, death is the ultimate
result). While Selye was not necessarily addressing exercise training in this stress
model, sports medicine professionals have used the GAS to describe training and the
resultant adaptations. Accordingly, when a short-term stressor is placed on the body,
super-compensation occurs as the disturbance in cellular homeostasis leads to adapta-
tions, and the athlete’s exercise performance is enhanced (10, 11). However, if too great
a stress or long-term stress occurs with insufficient recovery, then performance decre-
ments occur and overtraining results (3, 8, 12–14). A small window probably exists as
to when the stress and recovery are optimal, and a large window includes too little stress
for the recovery (i.e., undertraining or detraining resulting in nonoptimal performance)
and also too much stress and too little recovery (i.e., overtraining, also resulting in non-
optimal performance).
Short-term overtraining, often called overreaching, is generally considered to be an
appropriate component of training, typically lasts a few days to a couple of weeks
(8, 15–18), and results in fatigue probably due to insufficient metabolic recovery and
a temporary reduction in exercise performance (13, 18, 19). However, as the typical
response of an athlete and coach to reduced performance is that the training program
was not sufficient enough (i.e., that undertraining and/or detraining has occurred) and
greater training load must occur to enhance exercise performance, overreaching can be
expanded to overtraining due to lack of recovery and too much work. As very small
differences in exercise performance (i.e., speed of running or skating) generally leads
to great differences in exercise performance, athletes are always trying to get that last
little edge to enhance their performance time. To illustrate this, Snyder and Foster (20)
examined speed skater velocity at the 1988 Olympics and observed that there was
only a 0.3% difference in average velocity between all gold and silver medal perform-
ances and the mean difference between all first and fourth place finishers was only
1.3%. This difference in velocity covered races ranging from 0.5 to 15 min in length.
The overtraining syndrome has been shown to result in performance decrements of
0.7–15% (21) and to be similar to the exhaustion stage of Selye’s GAS model
(16, 22). The incidence of overtraining has ranged from approximately two-thirds of
elite distance runners (3, 16, 23, 24) to 20–50% of swimmers, basketball, soccer,
individual and team sport players (3, 21, 25–28), and military personnel (29).
Unfortunately, little is known about the adaptation process and the recovery needed
to maximize physiological adaptations and thus exercise performance (19). What may
work for one athlete may not work for another, as everyone responds to stress in a dif-
ferent manner (9): One athlete may adapt to a training program, while another may
have performance decrements due to overtraining on the same program (3, 13, 30). The
border between training adaptation and performance enhancements and overtraining
and performance decrements is not concrete, and probably involves other factors (or
stresses) than just exercise training (3, 13). In spite of this scientists have tried to iden-
tify markers of performance or physiological function that would enhance our ability
Chapter 27 / The Endocrine System in Overtraining 525

Typical symptoms of overtraining as shown by their prevalence in the reviewed literature
Impaired exercise performance
Increased ratings of perceived
exertion (RPE)
Increased incidence of infections
Change in appetite
Decreased muscular strength
Blood glucose levels during
exercise
Mineral depletion
Feelings of depression
Disturbances in mood
Lack of motivation
Table 1
Decreased reproductive
hormone levels
Normal submaximal and
decreased maximal lactate
levels
Elevated basal metabolic rate
Prolonged recovery
Heart rate recovery
Easily and chronically fatigued
Loss of competitive desire
Altered blood pressure
Exercising heart rate
Muscle soreness
Decreased maximal
oxygen uptake
Enzymatic markers
in blood
Decreased maximal
power output
Increased respiratory rate
Changes in body weight
Decreased efficiency of
movement
Resting heart rate
Increased irritability
Changes in sleep patterns
Loss of coordination

to train athletes (19). As such scientists have identified performance decrements,

exhaustion, changes in mood state, reduction in lactate threshold and workload at
4 mM lactate, maximal exercise reductions, and competitive incompetence among
others (see Table 1) as signs and/or symptoms of the overtraining syndrome.
However, many problems became apparent with the research and the literature con-
cerning overtraining of athletes. Initially, all excessive exercise training was termed
overtraining, staleness, or burnout; however, with some of these, recovery occurred
quickly (days), while with others recovery took much longer (weeks to months, possibly
years). Thus overreaching, an appropriate form of training with sufficient recovery, was
defined as excessive exercise training from which an athlete could recover in days to a
few weeks, while overtraining was excessive exercise training which required a much
longer period of recovery (31). However, unless one gives an athlete sufficient time to
recover, one does not know whether the athlete is overreached (probably a positive
training response) or overtrained (probably a negative training response)—as distin-
guishing between the two is very difficult (30). Therefore, in 2000 Budgett et al. (23)
proposed that the syndrome be called the “unexplained underperformance syndrome”
(UPS) as the term overtraining syndrome implied causation. Then in 2006 the European
College of Sports Science published a position statement which defined overreaching
and overtraining (8). As such, overtraining is the performance of strenuous exercise
training (thus a verb) that leads to overreaching or the overtraining syndrome.
Overreaching then can be short-term or functional overreaching as would be used in a
periodized training cycle or nonfunctional (or extreme) overreaching, that is moving in
the direction of the overtraining syndrome and requiring more recovery time (8, 32, 33).
The definitions bring to light that the physiological adaptations from training through
overreaching (functional to nonfunctional) to the overtraining syndrome occur on a
continuum, which is fluid and affected not just by exercise training but by other stresses
526 Snyder and Hackney

as well. Overreaching is generally perceived to be peripheral fatigue, while overtraining

syndrome is more of a central fatigue (3, 19, 34), and some have suggested that the
symptoms can be greater in athletes who are overreached than in those who have the
overtraining syndrome (8). Due to the time necessary to recover from the overtraining
syndrome and the ethical nature of the research area, most studies that have examined
the area of overtraining more than likely have only functionally or at the most nonfunc-
tionally overreached their subjects (8, 32).
The realization that overtraining probably has not been examined experimentally led
Halson and Jeukendrup (32) to ask “Does Overtraining Exist?” and in fact they state
very compelling arguments as to why it may not. Their arguments include that most
studies that have examined overtraining have not shown performance decrements, and
while it would seem intuitive that if a continuum occurs from training to overtraining,
that characteristics would change proportionally to training, this does not always hap-
pen. In addition, most studies do not have any baseline measurements for comparative
purposes, and great differences in the methods were used when performing the research.
From this, Halson and Jeukendrup (32) concluded that not much could be stated con-
clusively about overreaching and the overtraining syndrome, due to a lack of true
experimental studies in the area. These points and difficulties must be kept in mind
when examining the overtraining literature. Also, since few truly experimental studies
concerning overtraining and the overtraining syndrome are available in the literature,
this chapter uses more review articles than might be a normal practice to examine the
current state of the body of knowledge on the topic.

ENDOCRINE FUNCTION AND THE OVERTRAINING SYNDROME

As the endocrine system is very involved in physiological adaptations and recovery
to stress, much effort has been placed in examining hormone levels during different
periods of training. The results of this work are two hypothesized mechanisms by which
endocrine function affects exercise performance and may lead to the overtraining syn-
drome: sympathetic/parasympathetic imbalance and neuroendocrine dysfunction.
Since 1959, Israel (34) and later others (3, 13, 16, 19, 35, 36) have discussed two
forms of overtraining: the basedowoid and the addisonoid forms. While strict interpre-
tation of these terms would indicate that thyroid hyperfunction (morbus Basedow) and
adrenal hypofunction (morbus Addison) would occur, neither the thyroid nor the adre-
nal glands have been solely shown to be directly involved in the overtraining syn-
drome. Rather, it is hypothesized that the sympathetic system (basedowoid) is activated
during the early stages of overtraining, while in later stages of overtraining, the sym-
pathetic system is inhibited and the parasympathetic system (addisonoid) predomi-
nates (13, 22). The sympathetic form has also been associated more with high-intensity
explosive type sports such as sprinting, jumping, and throwing, while the parasympa-
thetic form has been thought to be more prevalent in distance athletes (4, 6, 13, 16, 19,
21, 36). While initially presented as two separate syndromes, current thinking is that
they are both part of a continuum which extends from training to overreaching to the
overtraining syndrome (2, 13, 16, 19, 21, 35), with the sympathetic form occurring
initially, then the sympathetic system is inhibited, leading to the parasympathetic form
Chapter 27 / The Endocrine System in Overtraining 527

(6, 19). As such, catecholamine levels have been examined in overtrained athletes with
decreases (16, 37, 38) and increases (3, 6, 21, 25, 39) or no change (40) observed.
Methodological problems (capillary vs. venous blood, half-life time, time of day, rela-
tionship to exercise, etc.) and intra-individual variability seem to cause this conflict in
the results and leave the use of catecholamine levels, and quite possibly other hormone
levels as well, problematic for the determination of the overtraining syndrome (8, 38,
41, 42). Similarly, as free catecholamine levels have been used as an indicator of over-
training, especially the sympathetic nervous system activity, plasma levels typically
only reflect an acute level (e.g., response to exercise), while 24-h urine levels would
give an indication of average activity for the day (4); thus the collection period greatly
affects the results and their interpretation. Finally, the type of exercise training may
affect the analysis as it has been suggested that volume-related overtraining may affect
hormone levels more than intensity-related overtraining (40, 43).
Under appropriate conditions, exercise training leads to adaptations which
stabilize the pituitary-adrenocortical system by lowering resting levels of the stress
hormones (2, 13). However, excessive exercise training has been hypothesized to
lead to neuroendocrine overload, which may result in any number of the overtraining
syndrome symptoms (2). Thus, hypothalamic-pituitary dysfunction has been hypoth-
esized with overtraining to disrupt the balance between anabolic (i.e., testosterone)
and catabolic (i.e., cortisol) hormones, and therefore may affect/prolong recovery
(13, 19, 44).
Adlercreutz et al. (45) suggested monitoring the ratio of testosterone to cortisol as a
means of examining this anabolic/catabolic balance in the athlete. Levels used to indi-
cate an overtrained state were a decrease of 30% in the testosterone/cortisol ratio or
values <0.035 (45). While some athletes have been identified with this technique (29,
45–48), many others have been observed to be overtrained by having met the specified
criteria, yet with no change in the testosterone/cortisol ratio (12, 18, 38, 44, 49–52).
Banfi and Dolci (53) observed that the ratio of free testosterone/cortisol was very useful
in monitoring professional soccer players, but the criterion values used, while decreased
from the control period, were much greater than the 0.035 proposed by Adlercreutz
et al. (45). Likewise, Hoogeveen and Zonderland (41) showed decreased levels of the
testosterone/cortisol ratio in heavily trained cyclists, but not to the levels proposed by
Adlercreutz et al. (45). Interestingly, Lane et al. (48) showed in cyclists during heavy
training that low daily dietary carbohydrate intake can induce a significant and substan-
tial (>40%) reduction in the free testosterone/cortisol ratio in as little as 4 days.
As such, cortisol levels in relation to the overtraining syndrome have been shown to
be both variable (54) and equivocal, with investigations showing no change (12, 15, 38,
44, 48–52, 55, 56), increases (14, 41, 46–48, 57), and decreases (14, 42, 54, 58) in the
values, and thus cortisol by itself seems to be a poor marker of overtraining (54).
Finally, while many studies of heavily trained athletes have shown decreased levels
of testosterone (29, 35, 41, 46–48, 50, 55, 59), not all studies have reported similar
results (12, 35, 38, 44, 49, 51, 52, 57). Even though regulation of testosterone levels is
primarily controlled by the hypothalamic-pituitary axis, low levels of testosterone in
overtrained males could be due to central (hypothalamic, pituitary) and/or peripheral
(i.e., reduced gonadal blood flow and/or adrenal overload) mechanisms.
528 Snyder and Hackney

For years, altered reproductive function has been known to occur in female athletes
(60–64), affecting anywhere from 6 to 79% of the athletes (63). Hypothalamic-pituitary
dysfunction has been one of the mechanisms that has received support for the develop-
ment of amenorrhea in female athletes (60–62, 64). While the overtraining syndrome has
not necessarily been associated with amenorrhea in female athletes (14), excessive train-
ing, especially in distance runners, has been discussed as well as and in combination with
chronic restricted and/or inadequate caloric intake (62–64). Reproductive function and/
or dysfunction in males is much more difficult to observe than that in females as the most
overt symptoms would include decreased libido and sperm count (59, 65).
Many other hormones have been examined in the hopes of providing a diagnostic
tool for determining the overtraining syndrome. As many of the symptoms of the over-
training syndrome are similar to central fatigue, 5-hydroxytryptamine (5-HT) has been
examined and/or indirectly assessed through a related hormone—prolactin (66).
Hackney et al. (65, 67, 68) and Bedgett et al. (66) observed that plasma prolactin release
was higher in overtrained athletes than in well-trained athletes, and thus these athletes
may have greater 5-HT receptor sensitivity. Resting and acute post-high-intensity resist-
ance exercise overtraining shows no changes in growth hormone levels (35). The hor-
mone leptin is known to regulate energy balance and suppress appetite (43, 69, 70); thus
it could also be a component of the overtraining syndrome. However, plasma leptin
levels were not changed with short term (8 days) strenuous training nor were changes
in leptin related to changes in plasma cortisol (which increased) and changes in the
testosterone to cortisol ratio (which decreased) (47). Changes in plasma leptin, however,
were significantly related (r = 0.596) to deceases in serum testosterone (47). Baylor and
Hackney (71) did report reduced leptin levels in some female rowers undergoing func-
tional overreaching, and this change was related to reductions in triiodothyronine (T3).
Since the testosterone/cortisol ratio has not been shown to be extremely reliable, Atlaoui
et al. (54) examined the 24-h urinary cortisol/cortisone ratio in elite swimmers and
observed that the ratio was related to exercise performance and tracked changes in the
training program. More research with this ratio may be warranted.
The exercise performance implications of the endocrine system changes that occur
with overtraining are incompletely understood, as discussed above. Some of the prob-
lems presented could be methodological. Others could be that the hormone levels of
each athlete are so individualized as is the athlete’s response/adaptations to their exer-
cise program that consensus information is not likely to occur. Food intake and compo-
sition can also alter the resting concentrations of a number of hormones as do stress and
diurnal and seasonal variations. The resultant conclusion from examining the literature
relative to the overtraining syndrome is that no one hormone can be tested to confirm or
refute the occurrence of the overtraining syndrome; thus single blood tests are not of
value in determining if the overtraining syndrome has occurred or not.
While single blood tests for hormone levels have not been found to be beneficial,
Meeusen and colleagues (5, 7) have tested a two-bout exercise protocol that has shown
significant differences between control, overreached, and athletes with the overtraining
syndrome. As one of the symptoms of overreaching and the overtraining syndrome is
fatigue and affected athletes can typically start a performance or practice at normal pace
but then have to reduce the pace due to the fatigue, Meeusen and colleagues (5, 7)
Chapter 27 / The Endocrine System in Overtraining 529

hypothesized that having athletes perform two maximal exercise tests would distinguish
between the different groups of athletes. To this end, a testing protocol was devised
which involved the subjects performing two incremental exercise tests to exhaustion 4 h
apart as might occur when subjects perform two workouts in a day. Blood samples were
then collected before and after each exercise bout and analyzed for hormone levels.
During the first exercise test the appropriately training athletes and the overreached
athletes had similar results both in respect to exercise performance and hormonal
responses (5). However, exercise performance during the second exercise bout was
decreased 3% in the appropriately trained subjects, 6% in the overreached subjects (fol-
lowing a training camp where training volume was increased 58%), and 11% in the
subject who reported to the laboratory with the overtraining syndrome (5). Hypothalamic-
pituitary hormone levels during the second test were likewise different between all three
groups, with the overtrained athletes’ hormone levels not increasing (5). During a sec-
ond study ten athletes who had decreased exercise ability performed the two-bout exer-
cise protocol (7). Retrospectively, five of the athletes were classified as nonfunctional
overreaching, and five of the athletes were classified with the overtraining syndrome
(7). While exercise performance was not different between the two groups of subjects,
following the second exercise bout, ACTH and prolactin levels were much higher for
the nonfunctional overreaching athletes than for the athletes with overtraining syn-
drome (who showed small or no increases in these hormone levels) (7). No appropri-
ately trained athletes were included in this second investigation. Collectively, the results
suggest that due to the fatigue associated with overreaching and the overtraining syn-
drome, the two-bout exercise protocol may be useful as a monitor of the two.
Unfortunately, the group differences were only distinguishable after the second exercise
bout to exhaustion, and performance in just one bout of exercise was not beneficial in
classifying the athletes. Thus, both exercise bouts seem to be needed for the protocol to
be diagnostic. However, since the two tests to exhaustion were performed within a very
short period of time (i.e., 4 h), repeated performance of this test throughout a training
season would need to be built into the training program regime, or if not it could add
excessively to the exercise training performed.

OTHER HYPOTHESIZED MECHANISMS OF THE OVERTRAINING

SYNDROME
Recently, two other mechanisms have been proposed related to the overtraining syn-
drome; one of these is the tissue trauma theory proposed by Smith (72, 73). Smith (72,
73) reviewed the current hypothesized mechanisms of the overtraining syndrome (such as
was done above) and then proposed that since none of these mechanisms totally explained
the overtraining syndrome, possibly these mechanisms function in response to trauma to
the tissue. Hence, trauma to the muscle, skeletal, and/or joint systems could be the initiator
of the overtraining syndrome. Exercise training and competition are known to result in
stress/injury of the tissue as part of the adaptive process (72, 73) as put forth by Selye (9)
many years ago. This trauma could be due to the eccentric nature of the exercise, the
increased energy needs, and/or ischemia, etc., which would result in mild inflammation as
adaptation occurred. With insufficient recovery any of these initial adaptive occurrences
530 Snyder and Hackney

could lead to a decrement in performance, the single most recognized sign of overtraining.
Thus, Smith (72, 73) hypothesized that exercise-induced microtrauma leads to local acute
inflammation which results in the release of cytokines. With increased training (high vol-
ume and/or high intensity) and insufficient recovery, the local acute inflammation is per-
petuated to local chronic inflammation and the enhanced level of cytokines released
results in activation of the circulating myocytes. The activated myocytes then produce
large quantities of proinflammatory cytokines, which leads to a systemic immune/
inflammatory response. The systemic inflammation is then proposed as the central cause
of the overtraining syndrome. The primary cytokines proposed to be involved with the
overtraining syndrome are IL-1b, TNF-a, and IL-6, though little research has been per-
formed with the overtraining syndrome and the cytokine levels (72, 73). The results of the
functions of these cytokines (e.g., mood change, loss of appetite, altered hormone levels—
decreased testosterone and increased cortisol, fatigue, decreased muscle mass, and
increased infection) are for the most part very similar to the symptoms of overreaching
and the overtraining syndrome, thus the proposed mechanism. More work needs to be
performed in this area to solidify this hypothesis, but it is interesting to note that elevated
prolactin is associated with proinflammatory mediators, and that previously mentioned
studies have reported increased prolactin in overtraining athletes (40, 46, 66, 68, 74).
Morgan et al. (24) initially drew the parallel between altered mood state and over-
reaching/the overtraining syndrome; however Armstrong and VanHeest (75) recently
connected the two more thoroughly. Armstrong and VanHeest (75), in examining both
the overtraining syndrome and major depressive disorder literature, observed that both
share common brain structures, immune responses, and endocrine pathways. Hence,
they proposed that the two shared a very similar mechanism. Morgan et al. (24) previ-
ously had observed that up to 80% of athletes with the overtraining syndrome had
significant mood changes and elevated levels of psychological depression. Part of this
mechanism could be that both depression and the overtraining syndrome have a dose–
response relationship with stressful events. Likewise, hypothalamic-pituitary dysfunc-
tion and an enhanced parasympathetic activity have been observed in depressed patients
(75). While many similarities exist, Armstrong and VanHeest (75) strongly recommend
that further research be performed in this area before antidepressant medications are
used with athletes who have the overtraining syndrome.

TRAINING CONSIDERATIONS TO PREVENT THE OVERTRAINING

SYNDROME
A decrement in exercise performance seems to be the only diagnostic standard of
overreaching and the overtraining syndrome (1, 8, 18, 32, 66, 76). Reduced perform-
ance ability is likely related to increased fatigue, but what causes the fatigue is not
known (40) though it may be related to tissue trauma and the activity of the cytokines
in response to inflammation as described by Smith (72, 73). Therefore, performance
testing is probably necessary to monitor fatigue and reduced performance, though the
type of test and its duration is currently not known (8, 32, 75).
Proper exercise training planning is critical in the prevention of overreaching and the
overtraining syndrome, as no one marker or measure has been observed to be a direct
indicator (13, 14, 16, 21, 22, 75–78). Acute overtraining/overreaching has been studied
Chapter 27 / The Endocrine System in Overtraining 531

by increasing training load (either volume or intensity) for 2–4 weeks, but this is not nor
should it be typical of normal training (78). Similarly, the risk of overtraining increases
after 3 weeks of intensified training or prolonged monotonous training (4). Therefore,
appropriately planned training programs using periodized training techniques (13, 30,
52) and varied training loads to avoid monotony in training (4, 16, 35, 77) are recom-
mended. With periodized training progressive increases in training intensity and/or vol-
ume occur for a given period (usually weeks), then a recovery period occurs. The pattern
then continues with progressive increases and recovery planned so that stress and adapta-
tion occur without overreaching or the overtraining syndrome (79, 80). While periodized
training is highly recommended to insure that adequate recovery occurs, very little
experimental research has been conducted on the results of periodized training. With
horses progressive increases in training loads were tolerated as long as sufficient recov-
ery time (i.e., moderate intensity endurance runs) occurred following the high-intensity
training days. When the high-intensity training days were not followed by recovery days,
the horses were observed to have symptoms of overtraining (76). In humans, as full
recovery from an intense exercise bout may require at least 48 h (2, 18), planned recov-
ery is necessary in a training program to insure that excessive training does not occur.
One method that might be useful in monitoring training is examination of the blood
lactate/rating of perceived exertion (RPE) ratio (81). Fatigue associated with overreach-
ing and the overtraining syndrome has resulted in higher submaximal RPE scores (40).
Conversely, while overreaching and the overtraining syndrome have not been shown to
alter submaximal blood lactate levels, maximal exercise blood lactate levels have
decreased (7, 20, 58, 81). Thus, decreases in the blood lactate/RPE ratio have been
shown to occur during periods of overtraining (40) and may be a simple way for
coaches and athletes to monitor training and recovery needs. However, further work is
necessary on this potentially useful biomarker.
Monitoring hormone levels of athletes during training is expensive, impractical, and
probably of questionable benefit (13, 18, 21, 38, 53, 66, 78, 82). Also, as hormone val-
ues generally are different between athletes, obtaining a single diagnostic value is very
difficult (82). At present, accessing the physiological responses to repeated maximal
bouts of exercise, either on 1 day or over multiple days, is probably the most helpful in
diagnosing overtraining syndrome (5, 7, 82) but also potentially adds to the excessive
stress of the exercise training program.
As suggested from the literature on amenorrheic female athletes, future work on the
causes of the overtraining syndrome may necessitate examining food intake (30),
specifically the amount of carbohydrates (48, 58, 83, 84) and protein (84–86) consumed.
Work on inflammation and the role of the cytokines as proposed in the theory of Smith
(72, 73) also would seem to be an appropriate future course of research.
As the difference in performance time between a gold medal and not medaling is
very small in most cases, most athletes are willing to train excessively to the point of
overtraining in order to prepare for competition, as most would rather become over-
trained and fail in their competition due to that than go into the competition not
sufficiently prepared. Thus coaches and athletes have to learn to adjust training when
increased physical and/or emotional stress is apparent to maximize the training adapta-
tions while reducing the probability of overreaching and/or the overtraining syndrome
occurring.
532 Snyder and Hackney

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